Module #4: Disorders of the Pulmonary System Flashcards
What is hypercapnia?
increase PaCO2 in arterial blood
What are some of the causes of hypercapnia?
Hypoventilation of alveoli
Supression of respiration centers (DRG/VRG)
Large airway obstructions (tumors/sleep apnea)
Damage to alveoli (emphysema)
Respiratory acidosis
What is tissue hypoxia
decreased O2 in ANY tissue
Define Hypoxemia
decreased PaO2 in arterial blood
What are the 5 major causes of hypoxemia?
Decreased PO2 of inspired air (altitude/suffocation)
Hypoventilation (meds that supress DRG/VRG)
Diffusion abnormality of alveolocapillary membrane (emphysema/fibrosis/edema)
Altered V/Q perfusion ratio (low or high)
What does low V/Q indicative of?
good perfusion (blood is getting to lungs fine) but inadequate ventilation
What does he mean by pulmonary “right to left shunting”?
Low V/Q
blood travels from RIGHT side of heart and returns to LEFT side of heart w/o receiving O2
What are some clinical examples (diseases) of right to left shunt
asthma
chronic bronchitis
pneumonia
ARDS (acute respiratory distress syndrome)
ARDS of infants (hyaline membrane disease
What does high V/Q indicative of?
inadequate blood flow in a well ventilated lung
What is a clinical example of a high V/Q?
pulmonary embolism
What is pulmonary aspiration?
entry of fluids/solids into trachea and lungs
What is pulmonary edema?
excess fluid in lungs
What is the most common cause of pulmonary edema?
heart disease (increased left sided pressures)
What is atelectasis?
collapse of lung tissue
What are the 4 types of atelectasis?
Compressive
Absorptive
Surfactant Impairment
Post-Op
What happens to cause compressive atelectasis?
external pressure compresses lung
caused by tumors, fluid/air in pleural space (pneumothrorax), abdominal distention
What happens to cause absorptive atelectasis?
air from blocked or hypo ventilated alveoli gets absorbed into system
How does surfactant impairment causes atelectasis?
lack of surfactant will increase surface tension and makes lungs prone to collapse
How is atelectasis prevented in post-op patients?
post-surgical deep breathing exercise
pt positioning
early ambulation (get them up and moving ASAP)
Define pneumothorax
air accumulation w/in pleural cavity (pleural space)
What are the 3 types of pneumothorax?
Open pneumothorax
Tension pneumothorax
Spontaneous pneumothorax
Describe what happens during an open pneumothorax
air enters pleural cavity during inspiration and exits during expiration
air pressure in pleural space now = barometric pressure
Describe what happens during tension pneumothorax
air enters plueral cavity during inspiration but DOES NOT EXIT during expiration
there is a gradual build up of air pressure in pleural space, it collapses lung and compresses/displaces other structures of mediastinum (heart/vessels/etc)
Describe what happens during spontaneous pneumothorax
an unexpected rupture of pleura
common in 20-40 yo males
may or may not develop into tension pneumothorax
What is pleural effusion?
fluid on pleural space
What could pleural effusion cause?
compressive atlectasis
What are some causes of fluid buildup?
transudate (water)
exudate (protein)
pus (infectious debris)
blood (hemothorax)
lymph fluid (chyle)
Define ARDS
acute respiratory distress syndrome due to acute inflammation and alveolar damage
Name some of the causes of ARDS
most common causes = infection (sepsis) or multiple trauma
also:
pneumonia
burns
aspiration
cardiopulmonary bypass surgery
pancreatitis
drug OD
smoke/toxic gas inhalation
radiation therapy
What are the 3 pathophysiology phases of ARDS
Phase 1: initial injury to lung leads to massive inflammatory response, surfactant is inactivated, alveoli collapse due to less compliance and filling of inflammatory fluid
Phase 2: Hyaline membrane forms into fibrous mass coating alveoli and bronchioles
Phase 3: respiratory failure, secondary systemic (throughout body) inflammatory response; damage other organs which may cause death
What are the 3 most common obstructive pulmonary diseases?
asthma
emphysema
chronic bronchitis
What is going on in the airway with obstructive pulmonary diseases?
airway obstruction that is worse w/ expiration
breath out = wheezy
airway expands during inspiration but collapses (recoils) during expiration
Name the clinical characteristics of obstructive pulmonary disease
Dyspnea = perceived difficulty of breathing
increased work of breathing (WOB)
wheezing
decreased FEV1/FVC ( blood can get to alveoli but lungs can’t deliver O2
What is COPD (chronic obstructive pulmonary disease/disorder)?
syndrome describes coexisting condition of chronic bronchitis and emphysema
What is the primary cause of COPD?
smoking
What is Chronic Bronchitis?
condition of excess mucous secretion and productive cough that lasts 3+ months and occurs 2 consecutive years
Describe the Pathophysiology of Chronic Bronchitis
bronchial tubes are narrowed –> “traps” air in distal lungs
excess mucous is produced in response to chronic exposure of irritants (smoke, pollution etc)
increased mucous impairs cilia –> increased risk of infection/inflammation
Low V/Q (blood is able to get to alveoli, but air can’t)
Hypoxemia (decreased PaO2 in arterial blood) –> increase in RBC # –> pulmonary hypertension –> cor pulmonale = hypertrophy (enlargement) and failure of right ventricle
Hypercapnia (increased PaCO2)
What are the clinical signs/symptoms of Chronic Bronchitis?
productive/persistent cough aka smokers cough
recurrent pulmonary infections
reduced flow rates (decreased FEV1/FVC <70%) = prolonged expiration
decreased FVC and increased RV
Name the treatments of Chronic Bronchitis
Expectorants
Bronchodilators
Physical Therapy (PT) = deep breathing exercises (pursed lip breathing)
Antibiotics and steroids (usually reserved for late stage of disease b/c of side effects)
Low flow O2 to address severe hypoxemia
What is the potential adverse effect of low flow O2 for chronic bronchitis?
Respiratory Depression
central chemoreceptors (DRG/VRG) are no longer sensitive due to chronic hypercapnia
peripheral receptors have taken over; these guys are sensitive to O2 pressure
if you give to much O2 and PaO2 rises above 60 mmHg, the peripheral receptors will depress ventilation
What is emphysema?
pathological accumulation of air in the lungs –> enlargement of acini (gas exchange airways)
Name and describe the 2 types of emphysema
Centriacinar (centrilobar) - destruction of bronchioles/alveolar ducts; alveolar sac remains intact
Panacinar (panlobular) - destruction of ENITRE acinus (terminal bronchiole, alveolar duct, alveoli)
Which type of emphysema is more common in chronic smokers?
Centriacinar (centrilobar) emphysema
Which type of emphysema is more common in the elderly?
Panacinar (panlobular) emphysema
Describe the pathophysiology of emphysema
lung tissue itself is damaged –> breakdown of elastin in septum of bronchioles, alveolar ducts and alveoli
destruction of acinus also damages pulmonary capillary beds
reduced elastin (connective tissue) limits the elastic recoil of lungs –> long slow expiration
What are the causes of emphysema?
Smoking
How does smoking effect the lungs to cause emphysema?
smoking inhibits production alpha1-antitrypsin (protease inhibitor) –> promotes the release and accumulation of elastase (enzyme that breaks down elastin (connective tissue protein) –> damages lung tissue
protease = enzyme that breaks down protein in normal tissue alpha1-antitrypsin inhibits elastase
smoking also favors the recruitment of WBC’s in the lungs
What are the clinical signs/symptoms of emphysema?
Early sign = dyspnea on exertion (DOE)
late sign = dyspnea at rest
NO COUGHING/WHEEZING
prolonged expiration
increased WOB
poor gas exchange –> hypoexmia (decreased PaO2) and hypercapnia (increased PaCO2)
Barrel chest = classic sign
Pts will sit leaned forward with arms extended to breath easier = classic breathing position
Decreased flow rates = FEV1/FVC <70%
FVC decreases
RV/TLC increase
End Stage = pulmonary hypertension and cor pulmonale (just like chronic bronchitis)
What are some of the acute treatments for emphysema?
O2 therapy
bronchodilators
corticosteroids/antibiotics
What are some of the chronic treatments for emphysema?
QUIT SMOKING
pulmonary PT –> pursed lipped breathing exercises and safe exercise strategies
O2 therapy (for hypoxemia
Beta agonist (dilate airways)
anticholinergic meds (prevent constriction of airways)
What is asthma?
reversible obstructive lung disease caused by increased reax of airways to various stimuli (hypersensitive)
Describe the pathophysiology of Asthma
Initial Attack:
Hyper responsiveness of the airways
stimulus (allergen) triggers massive inflammatory immune response –> inflammation and epithelial damage
3 classic pathological changes: bronchial smooth muscle spasm; mucous production (impair cilia function); vascular congestion
Late asthma response = secondary attack 4-12 hrs after due to infiltration of WBCs; can be more severe than initial attack
What are the clinical signs/symptoms of an asthma attack?
Audible high pitched wheezing (on either both inspiration and expiration or just expiration)
shortness of breath (SOB)
decreased flow rates (FEV1/FVC <70%)
increased respiration rate (tachypnea)
apprehension/anxiousness (dyspnea, tachycardia, sensation of chest constriction)
early on will have non-productive cough
later on will have productive cough (removes mucous)
What are some of the triggers of Asthma attacks?
Foods (wines)
Pollen
smoke
dust
mold
animals
pollutants
some are aspirin sensitive (NSAIDs)
Occupational hazards (wood dust, cotton dust, animals, etc)
Describe Exercise Induced Asthma (EIA)
symptoms
triggers
duration
onset 5 - 15 min after strenuous exercise
triggered especially in dry cold air (late fall)
lasts for 15-60 minutes
can just feel like you’re out of shape
could have “classic” asthma symptoms (SOB, wheezing, chest tightness, anxiety)
worse in “long duration endurace sports”
swimming is better (warm moist air)
What are the clinical signs/symptoms of restrictive pulmonary conditions?
short shallow breathing patterns
increased or no change in FEV1/FVC (>90%)
Decreased FVC, RV, TLC
dyspnea upon exercise progresses to dyspnea at rest
Name the 4 Restrictive Parenchymal Conditions
Sarcoidosis
Idiopathic pulmonary fibrosis
Pneumoconiosis
Drug or Radiation-induced interstitial lung disease
What is sarcoidosis?
inflammation that produces tiny lumps of cells in various organs throughout the body
microscopic lumps = granulomas
What are the 7 Restrictive Extraparenchymal Conditions?
Myasthenia gravis
Guillain-Barre syndrome
Muscular Dystrophies
C-spine Injuries
Kyphoscoliosis
Obesity
Ankylosing spondylitis
What is Pulmonary Fibrosis?
excessive fibrosis proliferation in the lungs
What are the causes of Pulmonary Fibrosis?
secondary complication from disease (TB/ARDS)
inhalation of environmental hazards (pneumoconiosis)
idiopathic pulmonary fibrosis
Describe the pathology of pulmonary fibrosis
Altered repair process leads to fibrosis and poor lung compliance
chronic inflammation
alveoli are invaded by fibroblasts –> shrink and lose elasticity
What is Pneumoconiosis?
lung pathology due to inhalation of inorganic environmental hazards (usually chronic exposure)
What are the most common inorganic environmental hazards that cause of Pneumoconiosis?
Silica –> mining
Asbestos
Coal Miner lung = combo of coal, silica, quartz
What causes TB?
mycobacterium tuberculosis
Describe the pathology of TB
inflammatory process is secondary to bacteria
immune response leads to formation of granulomatous lesions (tubercle)
tissue w/in tubercle becomes necrotic (caseous)
scar tissue forms around tubercle
m. tuberculosis remains dormant unless disrupted or if immune system becomes compromised (HIV)
What is the single greatest risk factor to reactive TB?
HIV
How would you diagnose TB?
Positive skin test- will indicated pt had disease or was vaccinated
Chest films - see calcifications/nodules in upper lobes of lungs
sputum culture - can take up to 6 wks
What is a pulmonary embolism?
blood clot
How are pulmonary emboli formed?
occlusion of pulmonary vascular/capillary supply
What happens to V/Q in pt w/ pulmonary embolism and what does that mean?
high V/Q ratio
lungs can deliver O2, but blood can’t get to alveoli
What is the most common pulmonary embolism?
Deep Vein Thrombosis (DVT)
What are the pathologic risk factors of pulmonary embolism?
Venous stasis - immobility (post-op/being old/travel/obesity), pregnancy, CHF
Hypercoagulation - congenital, oral contraceptives, malignancy
Damage to endothelium of blood vessels - trauma, surgery, CVA (stroke)
Describe the Pathology of pulmonary emboli
clots, fats, air can form emboli (big old clot)
emboli lodges in lungs
secondary response causes further vasoconstriction –> increase hypoxemia, increase pulmonary blood pressures –> right sided heart failure
vasoconstriction –> decreased surfactant production –> atelectasis –> hypoxemia
if massive enough can lead to cardiac arrhythmias, shock and death
